Evidence for other potential non-allergic mechanisms of action include, but may not be limited to, generation of cytokines such as TNF-alpha, IL-8 and reactive oxygen species [58], effects on lung dendritic cells [44] and IL-17 [59], [60], immunopathologic actions of C. pneumoniae-specific heat shock protein 60 [38], infection-induced bronchial ciliary dysfunction [61], bronchial epithelial damage [62] and other effects on lung structure [45]. The gene discussed is TNF; the disease is infection.